The present description relates to a fibrosis-causing agent.
Among a large variety of pulmonary diseases which hamper normal respiration is chronic obstructive pulmonary disease (COPD). It includes at least one of asthma, pulmonary emphysema, and chronic bronchitis, which occludes the lung. These diseases often give rise to their symptoms at one time, thereby making it difficult to determine which one of them causes lung occlusion in each case. COPD remains unchanged for several months and hence chronic bronchitis is clinically identified from the continued reduction of expiration for two or more years. The most serious symptoms relating to COPD are chronic bronchitis and pulmonary emphysema.
The pulmonary emphysema is characterized by an extraordinary expansion, accompanied by disorganization, of respiratory bronchioles, pulmonary alveoli, and alveolar sacs, which are collectively called alveolar parenchyma for gas exchange. The alveolar parenchyma in its normal state shrinks at the time of expiration; however, the enlarged alveolar parenchyma does not recover after expansion due to breathing. This prevents satisfactory expiration. Moreover, the pulmonary emphysema decreases the effective area of pulmonary alveoli and the number of capillary vessels running in all directions on the surface of pulmonary alveoli, which reduces the overall ventilating capacity of the lung. In addition, the lung suffering from pulmonary emphysema is poor in resilience and unable to keep the airway open by stretching because it has its elastin and collagen destroyed by inflammation. This makes the bronchus liable to deformation. The result is that as the lung shrinks for expiration the bronchus becomes narrow due to compression by its surrounding air-filled alveoli and the lung excessively expands, thereby preventing smooth expiration. This is the reason why patients with pulmonary emphysema expire breath while keeping their lips pursed up.
In Japan, there are about 50,000 patients with pulmonary emphysema, who receive home oxygen therapy. Moreover, those who are in the incipient or moderate stage of pulmonary emphysema are estimated to count up to about three million. The present medical treatment of pulmonary emphysema relies mostly on drug therapy and oxygen therapy. They are symptomatic therapies intended to alleviate or eliminate the symptom with the help of a bronchodilator which expands the bronchus to aid respiration. They are not necessarily effective. There are other therapies than mentioned above, such surgical ones as lung implantation, lung volume reduction surgery (LVRS), and bronchoscopic volume reduction (BVR). They still have many problems with great burdens on patients, poor prognosis (in the case of lung implantation), the possibility of pulmonary emphysema occurring in the remaining lung (in the case of LVSR), and limited past records proving effectiveness (in the case of BVR).
In contrast with the foregoing therapies, a new therapy we recently designed that reduces the lung capacity in a noninvasive manner. For example, JP-T-2009-514860 discloses a composition containing polycations and polyanions such that the ratio of X to Y is larger than about 1, where X denotes the product of the mass of polycations and the ratio of the electric charge per mass of polycations, and Y denotes the product of the mass of polyanions and the ratio of the electric charge per mass of polyanions. According to the disclosure, the composition promotes the localized pulmonary fibrosis in the lung's affected part, thereby achieving the lung volume reduction (LVR) and curing pulmonary emphysema (or COPD).